【摘要】 目的:考察麝香酮对谷氨酸引起PC12细胞损伤的保护作用及作用机制。方法:将大鼠嗜铬细胞瘤细胞株(pheochromocytom a cells,PC12)分为正常组、模型组、麝香酮10.0,1.0,0.1μmol.L-1高、中、低剂量组和1μmol.L-1尼莫地平组,用500μmol.L-1谷氨酸造成PC12细胞损伤,采用药物预处理给药方法,MTT法测定细胞存活率,流式细胞仪测定细胞凋亡率,采用Fura3/AM为荧光指示剂,用Vector21420多标记免疫分析仪研究麝香酮对谷氨酸所致损伤PC12细胞内Ca2+的作用,流式细胞仪检测线粒体跨膜电位,考察不同浓度麝香酮对PC12细胞的保护作用。结果:麝香酮可明显提高谷氨酸诱导的PC12细胞还原能力,抑制该细胞LDH的释放,提高细胞存活率;抑制兴奋性氨基酸所引起的细胞内Ca2+含量的升高;降低PC12细胞的凋亡百分率,并呈剂量相关性。结论:麝香酮可抑制谷氨酸诱导的PC12细胞凋亡,其作用机制可能与抑制细胞内钙超载,稳定细胞线粒体跨膜电位有关。更多还原

【Abstract】 Objective: To explore the mechanism of glutamate(Glu)-induced PC12 cell apoptosis and the protective effect of muscone.Method: PC12 cells were randomly divided into six groups: normal group(Normal),model group injured by glutamate(Glu),nimodipine group(Nim) and muskone groups(Mus) of high,middle and low doses.The PC12 cells were pretreated with or without different concentrations of muskone for 30 min and then exposed to glutamate.MTT assay for cell survival,flow cytometric detection of apoptotic cells,DCF assay for reactive oxygen species(ROS) and flow cytomet ric assay was performed to determine the mitochondrial membrane potential in PC12 cell.Result: PC12 cell damage,the concentrations of ,and apoptosis induced by Glu were decreased after being administrated with paeoniflorin.Conclusion: Muskone inhibited Glu-induced apoptosis in PC12 cells.The mechanism is related to inhibiting intracellular Ca2+ overload and maintaining mitochondral membrance potential.更多还原